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insulin, in women with PCOS, promotes increased 5-alpha reductase activity.  This results in a dysregulated HPA axis, promoting increased cortisol and androgen levels.

Mouse study finds that DHT metabolite provides negative feedback to HPA via 3beta androstaendiol.  What is interesting is that this signaling occurred through ER beta.  Androgen signaling processed through estrogen receptors.

This study found that lower TT and E1 associated with more "poor health" as defined by questionnaire.  The conclusion might lead one to think that Estrogen therapy is need in men.  Eightly percent of estrogen production in men occurs from Testosterone.  If Testosterone declines, then estrogen production will likewise decline.  A simple fact that the authors did not comment on.  Also, E1 binds with high affinity to ER alpha, which is pro-inflammatory and pro-proliferative: neither of which is a positive health benefit.   This appears to point more to a broad HPA suppression as an association to the "poor health".

Stress response in a animal model is blunted at the level of pituitary through a decrease in ACTH release and through increase in peripheral metabolism

peripheral aromatase activity and Testosterone to Estradiol production have central HPA axis suppression resulting in decreased LH and FSH and low Testosterone.

BPA shown to effect HPA in rats.  The effects were seen as a result of pre and post natal exposure of low dose bisphenol A.  Testosterone was not found to be negatively impacted.  

Adiponectin is negatively associated with LH, FSH production at the level of the pituitary and Testosterone at the level of the testicle.  Meaning: a risking adiponectin, as found in obesity, is associated with a down regulated HPA stimulation and Testosterone production.  This study, however, found a local autocrine/paracrine effect on sperm that was quite the opposite.

Myo-inositol improves PCOS.  Specifically, myo-inositol improved insulin sensitivity, reduced insulin levels and restored HPA function.  IN these women with amenorrhea and oligomenorrhea, menestrual cycle regularity was restored.

Interferon therapy in men with hepatitis C was found to decrease total Testosterone and Free Androgen index at the level of the gonads; this was independent of the HPA in this study.

Study of men with hepatitis C and interferon therapy found decrease in free and total Testosterone levels in men.  The study results suggest a non-HPA effect, which suggests more of a peripheral effect at the level of the TEsticles.

Only abstract available here, but low T is the result of primary (testicular failure) and/or secondary (HPA failure). 

Measurement and meaning of salivary cortisol: a focus on health and disease in children.

salivary cortisol used to evaluate HPA axis dysfunction, to predict fatigue, in breast cancer survivors

Declining Testosterone, calculated free Testosterone, Estradiol, and Estrone levels appear to be associated with muscle mass/strength decline in elderly men.  This points to a global decrease in HPA function rather than an individual, specific hormone deficiency.

Systemic illness i.e. inflammation is associated with impaired HPA function and gonadal function.  This can be translated as low T.  Low Testosterone is a biomarker of poor health in men.

Nice study that looked at climid to restore HPA function and increase Testosterone stimulation and production.  This study also does a good job of reviewing the mechanisms of low T.  Low T is really a biomarker of poor health in men.

Low T found in young combat veteran with PTSD and SI.  This is no surpass as there is significant HPA dysfunction in these men/women.  The overwhelming cortisol response and resultant PTSD will shut down endogenous Testosterone production.  I have seen this in several combat veterans.

Overtraining syndrome described.

Good case review of secondary adrenal insufficiency.  A common cause of low sodium and needs to be considered in elderly patients.  Also, low cortisol is associated with increased ADH.  In the case of adrenal insufficiency, the negative feed back of cortisol to the HPA is lost and recreation of CRH, which is an ADH secretagogue, will increase ADH secretion.

Great review on how stress effects the neuroimmunoendocrine systems.